Evidence map›Paper›PMID 28306077›Full record

ArticleRoux's archives of developmental biology : the official organ of the EDBO1995

Structure and regulation of the fushi tarazu gene from Drosophila hydei.

Wolfgang Jost, Yan Yu, Leslie Pick, Anette Preiss, Dieter Maier

Abstract read
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In one paragraph

Article in Roux's archives of developmental biology : the official organ of the EDBO, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 41% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Molecular heterochrony in the early development of Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Wolfgang JostBiozentrum der Universität Basel, Abt. Zellbiologie, Klingelbergstraße 70, CH-4056, Basel, Switzerland.
Yan YuBookdale Center for Molecular Biology, Mount Sinai School of Medicine, One Gustave L. Levy Place, BOX 1126, 10029, New York, NY, USA.
Leslie PickBookdale Center for Molecular Biology, Mount Sinai School of Medicine, One Gustave L. Levy Place, BOX 1126, 10029, New York, NY, USA.
Anette PreissBiozentrum der Universität Basel, Abt. Zellbiologie, Klingelbergstraße 70, CH-4056, Basel, Switzerland.
Dieter MaierBiozentrum der Universität Basel, Abt. Zellbiologie, Klingelbergstraße 70, CH-4056, Basel, Switzerland.
University of Basel · CHIcahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Drosophila melanogaster segmentation gene fushi tarazu (ftz) encodes a homeodomain-type transcription factor involved in the control of larval pattern formation. Loss of function mutations cause an embryonic lethal, pair-rule phenotype. The segmentation defects, but not the lethality, can be partially rescued by the ftz orthologue from Drosophila hydei. In this work, the primary structure, expression and regulation of the D. hydei ftz gene was characterized. Sequence comparisons classify ftz as a rather fast evolving gene. However, since the homeodomain of the D. hydei FTZ protein is highly similar to that of D. melanogaster, proper regulation of D. melanogaster ftz downstream genes would be expected. In D. melanogaster embryos, a D. hydei ftz transgene is expressed normally, independent of endogenous ftz gene activity, suggesting that D. hydei ftz regulatory sequences are correctly recognized by D. melanogaster transcription factors. Accordingly, lacZ fusion constructs driven by the D. hydei ftz upstream element are expressed normally in D. melanogaster embryos. Altogether, the similarities between the two ftz orthologues by far outweigh the differences. The limited success of the trans-species rescue might be, therefore, a consequence of the accumulation of too many subtle changes in gene function, exceeding the limits of developmental plasticity during fly embryogenesis.

Indexed as

DrosophilaEvolutionfzHomeodomainPlasticity

Identifiers

PMID28306077
OpenAlexW2053530443

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.